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Next Article 
Blood, Vol. 89 No. 10 (May 15), 1997:
pp. 3497-3501
EDITORIAL
Eosinophils and IgE Receptors: A Continuing Controversy
By
Hirohito Kita and
Gerald J. Gleich
From the Departments of Immunology and Medicine, Mayo Clinic and Mayo Foundation, Rochester, MN.
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ARTICLE |
DURING THE PAST 2 decades, considerable new information has been obtained about the functions of the eosinophil and its roles in human disease. Presently, the eosinophil is recognized as a proinflammatory granulocyte implicated in protection against parasitic infections and believed to play a major role in allergic diseases, such as bronchial asthma, allergic rhinitis, and atopic dermatitis.1 The eosinophil is an important source of cytotoxic cationic proteins, such as major basic protein (MBP), eosinophil peroxidase, and eosinophil cationic protein. These proteins are potentially two-edged swords; on the one hand, they protect the host against overwhelming helminth infections, but on the other hand, they damage the host's tissues.2 Eosinophils also induce inflammation by releasing lipid mediators, oxygen metabolites, and cytokines.2 Numerous studies have shown the association of eosinophils and various human parasitic and allergic diseases. For example, at present, the most common worldwide cause of eosinophilia is probably infection with helminths, and high eosinophil counts correlate with lack of reinfection after treatment of Schistosoma haematobium infections.3 Analyses of patients infected with Onchocerca volvulus have shown striking deposition of the eosinophil granule MBP around degenerating microfilaria.4 In allergic asthma, eosinophilic and lymphocytic infiltration in the epithelium and lamina propria of the airways are consistently found even in mild and stable asthma.5 Indeed, correlations have been observed between the numbers of infiltrating eosinophils and asthma disease severity.5 Pulmonary segmental allergen challenge in allergic individuals causes eosinophil recruitment into the airways; this is associated with the release of eosinophil granule proteins and the increase in vascular permeability.6,7 Despite the strong associations among eosinophils, their cytotoxic granule proteins, and human diseases, the mechanism(s) responsible for eosinophil activation in vivo is largely unknown.
Helminth infections and allergic diseases are characteristically associated not only with peripheral blood and tissue eosinophilia, but also with high levels of both total and antigen-specific IgE antibodies. IgE antibodies may be involved in disease in three ways. First, the central feature in anaphylactic and immediate hypersensitivity reactions is IgE-dependent activation of mast cells and basophils leading to the release of histamine and other inflammatory mediators, such as prostaglandins and leukotrienes.8 Furthermore, upon activation through IgE receptors, human mast cells and basophils produce cytokines, such as interleukin-4 (IL-4) and IL-5, which are potentially important in the recruitment of eosinophils, thus causing chronic allergic inflammation.9 Second, IgE bound to receptors on antigen-presenting cells, such as CD23 on B cells and to high-affinity IgE receptors (Fc RI) on Langerhans' cells and monocytes, can enhance antigen internalization and presentation to T cells, resulting in continuous activation of the immune system.10,11 Finally, IgE may mediate killing of the invading helminth and host cell damage by acting as a ligand for antibody-dependent cell-mediated cytotoxicity (ADCC) by macrophages and other immune cells.12 In fact, immunoepidemiological studies showed a significant correlation between the production of antischistosome IgE antibodies and the acquisition of immunity against reinfection to S haematobium.13 In allergic diseases such as bronchial asthma, there is a close correlation between serum IgE levels and the prevalence and severity of the diseases.14 Thus, there is now converging evidence to support roles for IgE in resistance to helminthic infections and in the pathophysiology of allergic diseases in humans. Therefore, it is reasonable to speculate that IgE is involved in the activation of eosinophils in these diseases.
Early studies on the killing of schistosomula in vitro by human eosinophils used cells purified from normal or slightly eosinophilic individuals, together with heat-inactivated sera from individuals with schistosome infection.15 The results of these studies suggested that killing requires IgG and is independent of complement. IgG1 and IgG3 subclasses were effective in mediating ADCC by human eosinophils, whereas IgM, IgG2, and IgG4 were not only inactive, but blocked the effects of the active subclasses.16 A quite separate phenomenon was observed with low density, so-called hypodense eosinophils that can be isolated from individuals with very high eosinophil counts. Receptors for IgE were identified on both rat and human hypodense eosinophils,17 and hypodense human eosinophils were shown to kill schistosomula in the presence of IgE.18 Subsequently, this human eosinophil IgE receptor was shown to be similar, but not identical, to the low-affinity IgE receptor (FcRII) expressed on B cells (CD23).19-23 Eosinophils from patients with eosinophilia express another low-affinity IgE-binding molecule belonging to the S-type lectin family, called Mac-2/ -binding protein.24 The cytotoxic function of eosinophils was abolished by the antibody against this molecule.24 More recently, in 1994, Gounni et al25 described FcRI on eosinophils from patients with marked eosinophilia. The evidence to support this claim was comprehensive and included the following: inhibition of [125I] IgE binding to eosinophils by anti-FcRI  -chain monoclonal antibody (clone 15.1); surface expression of FcRI -chain by flow cytometry; immunostaining of tissue eosinophils with 15.1; the demonstration of FcRI -,  -, and  -chain transcripts; release of eosinophil granule proteins after stimulation of eosinophils with 15.1; and inhibition of IgE-dependent eosinophil ADCC against schistosome targets by 15.1. Altogether, these findings suggest that human eosinophils express three receptors for IgE, namely FcRI, FcRII, and Mac-2, and that IgE induces eosinophil mediator release and ADCC through these receptors. Thus, on the basis of these reports, IgE-mediated activation of eosinophils was implicated as an important mechanism for host defense and in the pathophysiology of human disease.
However, the seemingly strong association between the eosinophil and disease becomes confusing and controversial in mice. For example, in helminth-infected animals, antibodies to IL-5 suppressed blood eosinophilia and eosinophil infiltration into the tissues. However, ablation of eosinophilia by anti-IL-5 was not associated with a diminution of resistance in mice infected with S mansoni26 or with Trichinella spiralis.27 Similarly, anti-IL-4 depletion of IgE responses failed to interfere with protective immunity to S mansoni.26 These findings suggest that neither eosinophils nor IgE are critical for immunity to these parasites in the mouse. In contrast, mice infected with Trichuris muris showed the exact opposite: their resistance to infection was associated with the production of Th2 cytokines, such as IL-4 and IL-5, tissue eosinophilia, and intestinal IgA production.28 In murine models of asthma using BALB/c mice sensitized and challenged with ovalbumin (OVA), one study showed that neither IL-5 nor eosinophils are required for airway hyperresponsiveness.29 In contrast, another study in which the C57BL/6 mice rendered IL-5 deficient by homologous gene recombination were sensitized and exposed to OVA, the animals failed to develop eosinophil infiltration into the lungs, airway hyperresponsiveness, and lung damage; their littermate controls showed all these responses.30 Reconstitution of IL-5 production with recombinant vaccinia viruses completely restored antigen-induced eosinophilia and airway dysfunction in these IL-5-deficient mice, suggesting a central role for IL-5 and eosinophilia in the pathogenesis of allergic lung disease. The inconsistencies among these murine disease models, as well as the inconsistencies between the human and mice findings, allows recognition of potential difference(s) between human and mouse eosinophilic leukocytes.
Previously, Lopez et al31,32 have described the distribution of Fc receptors on eosinophils isolated from mice infected with the cestode, Mesocestoides corti. In these reports, the investigators determined that murine eosinophils, similarly to human eosinophils, expressed the type II Fc receptor for IgG (Fc RII), but they were unable to detect any IgE binding to mouse eosinophils. More recently, Jones et al33 thoroughly examined eosinophils obtained by bronchoalveolar lavage (BAL) from the lungs of CBA/J mice infected with Toxocara cani by flow cytometry. They found that murine eosinophils are negative for surface IgM (sIgM), sIgA, sIgE, and FcRII, but are positive for sIgG1 and FcRII. Furthermore, they showed that culturing eosinophils for 24 or 48 hours with exogenous IgE and/or IL-4 did not induce IgE binding capacity or FcRII expression. In this issue of Blood, de Andres et al34 expand these studies considerably by including FcRI and Mac-2 and by examining mRNA transcripts and receptor-mediated cellular functions. de Andres et al34 examine murine eosinophils from two sources, namely eosinophils isolated from liver granuloma of CBA mice infected with S mansoni and bone marrow cells isolated from BALB/c mice and cultured with a combination of eosinophil growth factors. The results from these two different cell sources are virtually identical. Murine eosinophils lack IgE receptor expression; neither surface expression of FcRII or Mac-2 nor binding of murine IgE to the cells could be detected. Reverse transcription polymerase chain reaction (RT-PCR) analyses did not detect mRNA transcripts for the -chain of FcRI or FcRII, but did detect Mac-2 mRNA. In vitro culture of granuloma eosinophils did not induce IgE-binding or expression of IgE receptors. In contrast to the lack of IgE receptors, functioning IgG receptors, including FcRIIb and FcRIII, were detected on granuloma eosinophils, consistent with previous observations by others.
Studies of receptor expression have a number of potential pitfalls. For example, transcription of mRNA or even the presence of synthesized receptor protein within the cell does not necessarily indicate the expression of the receptor on cell surface.35 Another question concerns the potential discrepancies between receptor expression and actual functioning of the receptor. An antibody raised against an IgE receptor expressed on one cell type may not recognize the IgE receptor on another cell type, the best example being lack of binding of the antibody against human B-cell FcRII (CD23) to human eosinophils.23 Finally, precautions are needed to minimize or eliminate contamination by other cell types, particularly in highly sensitive RT-PCR analyses. The careful and well-designed study by de Andres et al34 published in this issue of Blood examined transcription of mRNA, surface receptor expression, IgE-binding capacity, and receptor-mediated cellular function; thus, they seem to address all of these potential problems. Their observations, together with previous reports by others, provide convincing evidence that murine eosinophils, seemingly unlike human eosinophils, lack IgE receptors. Therefore, murine eosinophils may use the FcR, complement receptors, and/or possibly Fc R in their antigen-dependent cellular functions; these may explain the differences between mouse and human observations and the discrepancies among findings made in mice.
The issues regarding expression of IgE receptors on mouse and human eosinophils deserve some comments and cautions. First, expression of IgE receptors on human eosinophils and their IgE-dependent functions are not phenomena commonly seen in eosinophils from all sources. Almost all the studies that showed the presence of IgE receptors on human eosinophils have used eosinophils from patients with marked eosinophilia, including the hypereosinophilic syndrome and diseases associated with skin disorders and lymphomas.18,19,24,25 There are no data to support expression of IgE receptors on eosinophilia from healthy donors and/or subjects with mild to moderate eosinophilia due to more common conditions, such as allergy and helminth infection. Three studies that sought IgE receptors in these conditions did not detect FcRII on peripheral blood eosinophils36,37 and detected only minimal levels of FcRI expression on eosinophils infiltrating into the bronchial tissues of patients with asthma38 and on blood eosinophils from patients with allergic rhinitis.37 Furthermore, IgE-dependent functions of eosinophils were not observed in blood eosinophils from normal individuals, whereas these eosinophils did respond vigorously to IgG1 and IgG3 through FcRII.16,39,40 Another level of complexity is added by the discrepancy between receptor expression and IgE-mediated cellular functions of eosinophils. Normal eosinophils, which fail to mediate IgE-dependent ADCC, do mediate such killing after activation with platelet-activating factor (PAF ) even in the absence of the expression of IgE receptors.41
Second, in association with the activation status issue described above, expression of IgE receptors on eosinophils may be tightly regulated by various environmental factors. For example, in humans the expression of FcRII was limited to eosinophils from persons with marked eosinophilia and, among them, to a unique cell population of hypodense eosinophils.19,42 Expression of the mRNA transcript for FcRI -chain was detected in peripheral blood eosinophils from patients with allergic rhinitis, but not in those from normal individuals.35 In addition, transcription of mRNA for FcRI -chain was enhanced by IL-4 in these human eosinophils,35 similar to results with human mast cells.43 The expression of FcRII is tightly regulated in a tissue-specific manner, and IL-4 again is the most potent inducer of FcRII expression for various types of cells.44 Therefore, those blood or tissue conditions with abundant IL-4 may favor the expression of IgE receptors on eosinophils. Because they used eosinophils isolated from an almost ideal source, namely liver granuloma of mice infected with S mansoni, the findings by de Andres et al34 are particularly informative. In addition to tissue and disease specificity, mice may also display another level of complexity. Because strains of mice differ greatly in their capacities to produce IL-4 and high levels of serum IgE,45 expression of IgE receptors on eosinophils may differ, depending on the strain. By using mice selected for heightened production of IgE, Eum et al46 concluded that the recruitment of eosinophils to the airways and high IgE titers are both required for lung pathology of allergic BP2 mice, and they speculated that IgE activation of eosinophils is important in this mouse model. It would be interesting if eosinophils from these animals were subjected to the rigorous analyses used by de Andres et al.34 Furthermore, van der Vorst et al47 reported the in situ localization of IgE cytophilic antibodies on murine eosinophils in the gut tissues of Swiss albino mice infected with Hymenlepis diminuta, although this study needs to be interpreted with caution due to the ubiquitous expression of IgE binding proteins in murine tissues.48 Thus, as summarized in Table 1, IgE receptor expression may be disease, tissue, species, and/or strain specific, and the observations obtained in a certain condition should not be generalized.
Finally, several published articles from investigators who studied human eosinophil IgE receptors need to be reconciled. In 1988, the eosinophil IgE receptor was originally found to have a low affinity (KD of 10-7 mol/L) and to possess a molecular weight corresponding to that of FcRII.20,42 IgE-binding and IgE-dependent ADCC to schistosomula were completely inhibited by antibody to either FcRII19 or Mac-2.24 Hence, earlier studies showed evidence for the expression of the low-affinity IgE receptor without any evidence for the high-affinity IgE receptor, FcRI. However, later in 1994, the same investigators reported the presence of FcRI on human eosinophils, and all of the IgE-dependent functions of human eosinophils were explained by this receptor.25 Again, IgE-dependent ADCC for schistosomula was essentially completely inhibited by antibody to FcRI, raising an obvious question as to how the IgE binding and ADCC can be totally inhibited by antibodies against three distinct IgE receptors. Thus, more confirmatory work is needed to finally resolve the presence or absence of IgE receptors on human eosinophils, as well as on mouse eosinophils.
In conclusion, with the recent development of techniques to manipulate genes and with the increased availability of a wide variety of immunologic reagents for mice, the numbers of murine models of human immunity and disease have strikingly increased. The studies by de Andres et al34 in this issue of Blood warn us of potential cellular differences between mouse and human immunologic responses and encourage us to reexamine the suitability of mouse models for human diseases. At the same time, their report raises unanswered questions regarding the expression of IgE receptors on human eosinophils. Further studies on IgE receptors on mouse and human eosinophils may solve the existing controversies and help to interpret and to understand the pathophysiologic mechanisms of human eosinophilic disorders, the roles of eosinophils in human immunity, and their murine models.
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FOOTNOTES |
Address reprint requests to Hirohito Kita, MD, Department of Immunology, Mayo Clinic, 200 First St SW, Rochester, MN 55905.
The publication costs of this article were defrayed in part by page
charge payment. This article must therefore be hearly marked
``advertisment'' in accordance with 18 U.S.C. section 1734 solely to
indicate this fact.
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REFERENCES |
1. Butterfield JH, Leiferman KM, Gleich GJ: Eosinophil-associated diseases, in Frank MM, Austen KF, Claman HN, Unanue ER (eds): Samter's Immunologic Diseases. Boston, MA, Little Brown and Co, 1995, p 501
2. Gleich GJ, Kita H, Adolphson CR: Eosinophils, in Frank MM, Austen KF, Claman HN, Unanue ER (eds): Samter's Immunologic Diseases. Boston, MA, Little Brown and Co, 1995, p 205
3.
Hagan P,
Wilkins HA,
Blumenthal UJ,
Hayes RJ,
Greenwood BM:
Eosinophilia and resistance to Schistosoma haematobium in man.
Parasite Immunol
7:625,
1985[Medline]
[Order article via Infotrieve]
4.
Kephart GM,
Gleich GJ,
Connor DH,
Gibson DW,
Ackerman SJ:
Deposition of eosinophil granule major basic protein onto microfilariae of Onchocerca volvulus in the skin of patients treated with diethylcarbamazine.
Lab Invest
50:51,
1984[Medline]
[Order article via Infotrieve]
5.
Bousquet JB,
Chanez P,
Lacoste JY,
Barneon G,
Ghavanian N,
Enander I,
Venge P,
Ahlstedt S,
Simony-Lafontaine J,
Godard P,
Michel FB:
Eosinophilic inflammation in asthma.
N Engl J Med
323:1033,
1990[Abstract]
6.
Sedgwick JB,
Calhoun WJ,
Gleich GJ,
Kita H,
Abrams JS,
Schwartz LB,
Volovitz B,
Ben-Yaakov M,
Busse WW:
Immediate and late allergic airway response to segmental antigen. Characterization of eosinophil and mast cell mediators.
Am Rev Respir Dis
144:1274,
1991[Medline]
[Order article via Infotrieve]
7.
Collins DS,
Dupuis R,
Gleich GJ,
Bartemes KR,
Ko YY,
Pollice M,
Albertine KH,
Fish JE,
Peters SP:
Immunoglobulin E-mediated increase in vascular permeability correlates with eosinophilic inflammation.
Am Rev Respir Dis
147:677,
1993[Medline]
[Order article via Infotrieve]
8.
Galli SJ,
Gordon JR,
Wershil BK:
Cytokine production by mast cells and basophils.
Curr Opin Immunol
3:865,
1991[Medline]
[Order article via Infotrieve]
9.
Bradding P,
Roberts JA,
Britten KM,
Montefort S,
Djukanovic R,
Mueller R,
Heusser CH,
Howarth PH,
Holgate ST:
Interleukin-4, -5, and -6 and tumor necrosis factor- in normal and asthmatic airways: Evidence for the human mast cell as a source of these cytokines.
Am J Respir Cell Mol Biol
10:471,
1994[Abstract]
10.
Mudde GC,
Bheekha R,
Bruijnzeel-Koomen CAFM:
IgE-mediated antigen presentation.
Allergy
50:193,
1995[Medline]
[Order article via Infotrieve]
11.
Maurer D,
Fiebiger E,
Ebner C,
Reininger B,
Fischer GF,
Wichlas S,
Jouvin MH,
Schmittegenolf M,
Kraft D,
Kinet JP,
Stingl G:
Peripheral blood dendritic cells express FcRI as a complex composed of FcRI- and FcRI-chains and can use this receptor for IgE-mediated allergen presentation.
J Immunol
157:607,
1996[Abstract]
12.
Capron A,
Dessaint JP,
Haque A,
Capron M:
Antibody-dependent cell-mediated cytotoxicity against parasites.
Prog Allergy
31:234,
1982[Medline]
[Order article via Infotrieve]
13.
Hagan P,
Blumenthal UJ,
Dunn D,
Simpson AJG,
Wilkins HA:
Human IgE, IgG4 and resistance to reinfection with Schistosoma haematobium.
Nature
349:243,
1991[Medline]
[Order article via Infotrieve]
14.
Sears MR,
Burrows B,
Flannery EM,
Herbison GP,
Hewitt CJ,
Holdaway MD:
Relation between airway responsiveness and serum IgE in children with asthma and in apparently normal children.
N Engl J Med
325:1067,
1991[Abstract]
15.
Butterworth AE,
Sturrock RF,
Houba V,
Mahmoud AA,
Sher A,
Rees PH:
Eosinophils as mediators of antibody-dependent damage to schistosomula.
Nature
256:727,
1975[Medline]
[Order article via Infotrieve]
16.
Khalife J,
Dunne DW,
Richardson BA,
Mazza G,
Thorne KJI,
Capron A,
Butterworth AE:
Functional role of human IgG subclasses in eosinophil-mediated killing of schistosomula of Schistosoma mansoni.
J Immunol
142:4422,
1989[Abstract]
17.
Capron M,
Capron A,
Dessaint JP,
Torpier G,
Johansson SGO,
Prin L:
Fc receptors for IgE on human and rat eosinophils.
J Immunol
126:2087,
1981[Medline]
[Order article via Infotrieve]
18.
Capron M,
Spiegelberg HL,
Prin L,
Bennich H,
Butterworth AE,
Pierce RJ,
Ouaissi MA,
Capron A:
Role of IgE receptors in effector function of human eosinophils.
J Immunol
132:462,
1984[Abstract]
19.
Capron M,
Jouault T,
Prin L,
Joseph M,
Ameisen JC,
Butterworth AE,
Papin JP,
Kusnierz JP,
Capron A:
Functional study of a monoclonal antibody to IgE Fc receptor (FcR2) of eosinophils, platelets, and macrophages.
J Exp Med
164:72,
1986[Abstract/Free Full Text]
20.
Jouault T,
Capron M,
Balloul JM,
Ameisen JC,
Capron A:
Quantitative and qualitative analysis of the Fc receptor for IgE (FcRII) on human eosinophils.
Eur J Immunol
18:237,
1988[Medline]
[Order article via Infotrieve]
21.
Grangette C,
Gruart V,
Ouaissi MA,
Rizvi F,
Delespesse G,
Capron A,
Capron M:
IgE receptor on human eosinophils (FcRII). Comparison with B cell CD23 and association with an adhesion molecule.
J Immunol
143:3580,
1989[Abstract]
22.
Yokota A,
Kikutani H,
Tanaka T,
Sato R,
Barsumian EL,
Suemura M,
Kishimoto T:
Two species of human Fc receptor II (FcRII/CD23): Tissue-specific and IL-4-specific regulation of gene expression.
Cell
55:611,
1988[Medline]
[Order article via Infotrieve]
23.
Capron M,
Truong MJ,
Aldebert D,
Gruart V,
Suemura M,
Delespesse G,
Tourvieille B,
Capron A:
Heterogeneous expression of CD23 epitopes by eosinophils from patients. Relationships with IgE-mediated functions.
Eur J Immunol
21:2423,
1991[Medline]
[Order article via Infotrieve]
24.
Truong MJ,
Gruart V,
Liu FT,
Prin L,
Capron A,
Capron M:
IgE-binding molecules (Mac-2/BP) expressed by human eosinophils. Implication in IgE-dependent eosinophil cytotoxicity.
Eur J Immunol
23:3230,
1993[Medline]
[Order article via Infotrieve]
25.
Gounni AS,
Lamkhioued B,
Ochiai K,
Tanaka Y,
Delaporte E,
Capron A,
Kinet JP,
Capron M:
High-affinity IgE receptor on eosinophils is involved in defence against parasites.
Nature
367:183,
1994[Medline]
[Order article via Infotrieve]
26.
Sher A,
Coffman RL,
Hieny S,
Cheever AW:
Ablation of eosinophil and IgE responses with anti-IL-5 or anti-IL-4 antibodies fails to affect immunity against Schistosoma mansoni in the mouse.
J Immunol
145:3911,
1990[Abstract]
27.
Herndon FJ,
Kayes SG:
Depletion of eosinophils by anti-IL-5 monoclonal antibody treatment of mice infected with Trichinella spiralis does not alter parasite burden or immunologic resistance to reinfection.
J Immunol
149:3642,
1992[Abstract]
28.
Else KJ,
Hultner L,
Grencis RK:
Cellular immune responses to the murine nematode parasite Trichuris muris. II. Differential induction of TH-cell subsets in resistant versus susceptible mice.
Immunology
75:232,
1992[Medline]
[Order article via Infotrieve]
29.
Corry DB,
Folkesson HG,
Warnock ML,
Erle DJ,
Matthay MA,
Wiener-Kronish JP,
Locksley RM:
Interleukin 4, but not interleukin 5 or eosinophils, is required in a murine model of acute airway hyperreactivity.
J Exp Med
183:109,
1996[Abstract/Free Full Text]
30.
Foster PS,
Hogan SP,
Ramsay AJ,
Matthaei KI,
Young IG:
Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model.
J Exp Med
183:195,
1996[Abstract/Free Full Text]
31.
Lopez AF,
Strath M,
Sanderson CJ:
Mouse immunoglobulin isotypes mediating cytotoxicity of target cells by eosinophils and neutrophils.
Immunology
48:503,
1983[Medline]
[Order article via Infotrieve]
32.
Lopez AF,
Battye FL,
Vadas MA:
Fc receptors on mouse neutrophils and eosinophils: Antigenic characteristics, isotype specificity and relative cell membrane density measured by flow cytometry.
Immunology
55:125,
1985[Medline]
[Order article via Infotrieve]
33.
Jones RE,
Finkelman FD,
Hester RB,
Kayes SG:
Toxocara canis: Failure to find IgE receptors (FcR) on eosinophils from infected mice suggests that murine eosinophils do not kill helminth larvae by an IgE-dependent mechanism.
Exp Parasitol
78:64,
1994[Medline]
[Order article via Infotrieve]
34.
de Andres B,
Rakasz E,
Hagan M,
McCormick ML,
Mueller AL,
Elliot D,
Metwali A,
Sandor M,
Britigan BE,
Weinstock JV,
Lynch RG:
Lack of Fc- receptors on murine eosinophils: Implication for the functional significance of elevated IgE and eosinophils in parasitic infections.
Blood
89:3826,
1997[Abstract/Free Full Text]
35.
Terada N,
Konno A,
Terada Y,
Fukuda S,
Yamashita T,
Abe T,
Shimada H,
Ishida K,
Yoshimura K,
Tanaka Y,
Ra C,
Ishikawa K,
Togawa K:
IL-4 upregulates Fc epsilon RI alpha-chain messenger RNA in eosinophils.
J Allergy Clin Immunol
96:1161,
1995[Medline]
[Order article via Infotrieve]
36. Hartnell A, Walsh GM, Moqbel R, Kay AB: Phenotypic marker on human eosinophils. J Allergy Clin Immunol 83:192, 1989 (abstr)
37. Kita H, Kaneko M, Frigas E, Bartemes KR, Weiler DA, Gleich GJ: Eosinophils from hay fever patients degranulate in response to IgG, but not to IgE. J Allergy Clin Immunol 95:339, 1995 (abstr)
38.
Humbert M,
Grant JA,
Taborda-Barata L,
Durham SR,
Pfister R,
Menz G,
Barkans J,
Ying S,
Kay AB:
High-affinity IgE receptor (FcRI)-bearing cells in bronchial biopsies from atopic and nonatopic asthma.
Am J Respir Crit Care Med
153:1931,
1996[Abstract]
39.
Kaneko M,
Swanson MC,
Gleich GJ,
Kita H:
Allergen-specific IgG1 and IgG3 through Fc gamma RII induce eosinophil degranulation.
J Clin Invest
95:2813,
1995
40.
Butterworth AE,
Remold HG,
Houba V,
David JR,
Franks D,
David PH,
Sturrock RF:
Antibody-dependent eosinophil-mediated damage to 51Cr-labeled schistosomula of Schistosoma mansoni: Mediation by IgG, and inhibition by antigen-antibody complexes.
J Immunol
118:2230,
1977[Abstract/Free Full Text]
41.
Moqbel R,
Walsh GM,
Nagakura T,
MacDonald AJ,
Wardlaw AJ,
Iikura Y,
Kay AB:
The effect of platelet-activating factor on IgE binding to, and IgE-dependent biological properties of human eosinophils.
Immunology
70:251,
1990[Medline]
[Order article via Infotrieve]
42.
Capron M,
Grangette C,
Torpier G,
Capron A:
The second receptor for IgE in eosinophil effector function.
Chem Immunol
47:128,
1989[Medline]
[Order article via Infotrieve]
43.
Toru H,
Ra C,
Nonoyama S,
Suzuki K,
Yata J,
Nakahata T:
Induction of the high-affinity IgE receptor (FcRI) on human mast cells by IL-4.
Int Immunol
8:1367,
1996[Abstract/Free Full Text]
44.
Delespesse G,
Sarfati M,
Wu CY,
Fournier S,
Letellier M:
The low-affinity receptor for IgE.
Immunol Rev
125:77,
1992[Medline]
[Order article via Infotrieve]
45.
Rizzo LV,
Umetsu DT,
DeKruyff RH:
Differential regulation of antigen presentation in high- and low-IgE responder mice.
Eur J Immunol
21:1767,
1991[Medline]
[Order article via Infotrieve]
46.
Eum SY,
Haile S,
Lefort J,
Huerre M,
Vargaftig BB:
Eosinophil recruitment into the respiratory epithelium following antigenic challenge in hyper-IgE mice is accompanied by interleukin 5-dependent bronchial hyperresponsiveness.
Proc Natl Acad Sci USA
92:12290,
1995[Abstract/Free Full Text]
47.
Van der Vorst E,
Dhont H,
Cesbron JY,
Capron M,
Dessaint JP,
Capron A:
Influence of an Hymenolepis diminuta infection on IgE and IgA bound to mouse intestinal eosinophils.
Int Arch Allergy Appl Immunol
87:281,
1988[Medline]
[Order article via Infotrieve]
48.
Gritzmacher CA,
Robertson MW,
Liu FT:
IgE-binding protein: Subcellar localization and gene expression in many murine tissues and cells.
J Immunol
141:2801,
1988[Abstract]
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